week 2 Flashcards

1
Q

Describe 3 theories of ageing

A

Rate-of-Living Theories

Cellular Theories

Programmed cell death theories

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2
Q

What is ageing?

A

The accumulation of changes in a human being over time; physical, psychological and social

‘The collection of changes that render human beings progressively more likely to die’ (Medawar, 1952)

After our sexual peak (about 30), our chances of dying double approximately every 8 years (MDRT)

The rate of ageing and the MRDT are thought to have remained unchanged for thousands of years

The mortality rate (IMR) has been lowered – meaning an increase in lifespan and longevity

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3
Q

What is ageing? (3 things)

A

Primary ageing is normal, disease-free development during adulthood.

Secondary ageing is developmental changes that are related to disease, lifestyle, and other environmentally induced changes that are not inevitable (e.g., pollution).

Tertiary ageing is the rapid losses that occur shortly before death

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4
Q

What is MRDT?

A

Mortality Rate Doubling Time:

After our sexual peak (about 30), our chances of dying double approximately every 8 years

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5
Q

What is IMR

A

the initial mortality rate

the mortality rate independent of aging, often calculated from the mortality rate prior to its exponential increase with age;

What happened last century was that the IMR, which is not affected by the aging rate, was lowered due to breakthroughs in different areas, such as in the war against infectious diseases, thus lowering mortality rates across the entire lifespan and increasing the life expectancy. Because the increase in life expectancy was due to changes in the IMR independent of changes in aging rates is also the reason why the average lifespan of humans may be reaching a plateau.

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6
Q

Reasons why we age

A

Programmed factors - ageing follows a biological timetable which is driven by genetically regulated processes

Damage-related factors - ageing results from a continuous process of damage accumulation originating in by-products of metabolism

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7
Q

Rate-of-Living Theories

A

The faster an your metabolism, the shorter your lifespan

  • Limited energy
  • Hormonal regulatory system adaptation to stress
  • Excess calories
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8
Q

Cellular Theories

A

Limited number of times a cell can divide Hayflick limit
-Telomeres and the enzyme telomerase

Wear and tear
-Tissues become worn out

Cross-linking
-Tissue becomes stiffer with age

Free radicals
-Reactive chemicals causing cellular damage

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9
Q

Programmed cell death theories

A

Aging may be programmed into genetic code

Cells pre-programmed to self-destruct
-Apoptosis- genetically motivated process ofprogrammed cell death where acell iscarefully sectionalized and its fragments can beused byother cells asabuilding material

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10
Q

Genes and ageing

A

Genes can increase or decrease longevity in complicated ways
A single gene mutations in worms can extend lifespan by almost 10-fold
There is a significant degree of heritability of longevity, in particular at later ages
The offspring of long-lived parents are protected against age-related diseases

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11
Q

Progeroid syndromes

A

Rare genetic diseases that manifest in ‘accelerated ageing’

Werner’s (WS), Cockayne, and Hutchinson-Gilford’s (progeria) syndrome

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12
Q

Ageing is a complex process composed of several features:

A

An exponential increase in mortality

Physiological changes that typically lead to a functional decline with age

Increased susceptibility to certain diseases

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13
Q

Life Expectancy:

A

How long one is expected to live

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14
Q

Longevity

A

The period of time one is expected to live under ideal circumstances

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15
Q

Lifespan

A

The period of time in which life events typically occur

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16
Q

Somesthesia and Balance

A

the perception of tactual or proprioceptive or gut sensations; “he relied on somesthesia to warn him of pressure changes”

17
Q

The Skin:

A
Loss of elasticity
Discoloration
Surface damage
Lessened sweat and oil gland production
Loss of subcutaneous fat
18
Q

hair

A

Graying from cessation of pigmentation

Loss from destruction of germination centers

19
Q

height

A

Loss of height due to shrinking of vertebrae
Weight gain then loss
Redistribution of body fat

20
Q

Muscles

A

Sarcopenia
Loss of muscle mass

after 40s/50s loss of 12-15% strength
per decade

21
Q

Loss of Bone Strength

A

Due to relative increase in bone destruction compared to growth of tissue

Because of decrease in bone mineral content of 5-12% per decade from 20s-90s

22
Q

Psychological Implications

A
Looking and bodily “feeling” old
			Identity (self concept)
			Identity (viewed by others-ageism)
			Independence (daily living)
Prompt: Age-related control behaviors	(+/-)
Prompt: Ergonomic design issues
23
Q

Vision

A

Due to structural changes
older need more light
increased sensitivity to glare
dark and light adaptation takes longer
poorer colour discrimination for short wave lengths
focussing near-far and far-near takes longer
presbyopia

24
Q

Presbycusis

A

=inability to hear high-pitched tones

25
Q

The 3 major changes in the brain with aging

A

Neurons
Neurotransmitters
Brain structure

26
Q

Neurons and ageing

A
Number of neurons declines
Number and size of dendrites decreases
Tangles develop in axon fibers
Increases in deposits of proteins
Number of synapses decreases
27
Q

Neurotransmitters and aging

A

Dopamine is associated with higher–level cognitive functioning, so declines are related to poorer:
Serotonin and acetylcholine also decline with age

28
Q

Brain structure and ageing

A

White matter hyperintensities (WMH)
Indicates myelin loss or neural atrophy
Considerable shrinkage occurs in the brain
Especially in prefrontal cortex, hippocampus and cerebellum
Diffusion tensor imaging (DTI)
Provides index of density or structural health of the white matter

29
Q

Impacts of brain changes

A

Executive Functioning
Difficulty focusing solely on relevant information
Due to WMH and reduced volume of prefrontal cortex
Memory
Specific structural changes (e.g., the hippocampus) result in memory decline
Emotion
Increased processing of positive emotional information with age
Better emotion regulation with age

30
Q

Explaining age related brain changes

A

The Parieto-Frontal Integration Theory (P-FIT)
HAROLD (hemispheric asymmetry reduction in older adults
CRUNCH (compensation-related utilization of neural circuits hypothesis)
STAC (scaffolding theory of cognitive age)

31
Q

Implications of the Developmental Forces

A

Unified theory not yet developed
Three general approaches to slowing or reversing the aging process:
Delay the chronic illnesses of old age
Slow the fundamental processes of aging to increase life span
Arrest or reverse aging by removing the damage caused by the metabolic process